The AreA transcription factor in Fusarium graminearum regulates the use of some nonpreferred nitrogen sources and secondary metabolite production

The AreA transcription factor in Fusarium graminearum regulates the use of some nonpreferred nitrogen sources and secondary metabolite production
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DOI:
10.1016/j.funbio.2013.10.006
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发表时间:
2013-11-01
期刊:
影响因子:
2.5
通讯作者:
Sorensen, Jens Laurids
Sorensen, Jens Laurids
中科院分区:
生物学3区
文献类型:
--
作者:
Giese, Henriette;Sondergaard, Teis Esben;Sorensen, Jens Laurids

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已知生长条件会影响丝状真菌次生代谢物的产生。研究了不同氮源和转录因子面积对禾谷镰刀菌真菌毒素产生的影响。谷氨酰胺和氨氮源对小麦赤霉病菌生长不利,天冬酰胺是小麦赤霉病菌的优先氮源。areA缺失导致NaNO3生长不良,提示其参与硝酸盐还原过程的调控。此外,天冬氨酸、组氨酸、异亮氨酸、亮氨酸、苏氨酸、酪氨酸和缬氨酸作为氮源的利用取决于一个功能区。研究表明,无论营养培养基如何,霉菌毒素脱氧雪腐镰刀菌烯醇(DON)、玉米赤霉烯酮和镰刀菌素H的产生都需要面积。在氮充足的条件下,缺失AreA的抑制因子nmr对其生长和产毒均无明显影响。区域似乎直接或间接地调节一些真菌毒素的产生,不依赖于氮的状态,并在某些氨基酸的利用中发挥作用。(C) 2013英国真菌学学会。Elsevier Ltd.出版。版权所有。
Growth conditions are known to affect the production of secondary metabolites in filamentous fungi. The influence of different nitrogen sources and the transcription factor AreA on the production of mycotoxins in Fusarium graminearum was examined. Growth on glutamine or NH4-sources was poor and asparagine was found to be a preferential nitrogen source for F. graminearum. Deletion of areA led to poor growth on NaNO3 suggesting its involvement in regulation of the nitrate reduction process. In addition utilization of aspartic acid, histidine, isoleucine, leucine, threonine, tyrosine, and valine as nitrogen sources was shown to depend of a functional AreA. AreA was shown to be required for the production of the mycotoxins deoxynivalenol (DON), zearalenone, and fusarielin H regardless of the nutrient medium. Deletion of nmr, the repressor of AreA under nitrogen sufficient conditions, had little effect on either growth or toxin production. AreA appears to regulate production of some mycotoxins directly or indirectly independent on nitrogen status and plays a role in utilization of certain amino acids. (C) 2013 The British Mycological Society. Published by Elsevier Ltd. All rights reserved.